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• W2163675591 abstract "Background . Exclusive enteral nutrition (EEN) is a well-established approach to the management of Crohn’s disease. Aim . To determine effects of EEN upon inflammation and gut barrier function in a colitis mouse model. Methods . Interleukin-10-deficient mice (IL-10 −/− ) were inoculated with Helicobacter trogontum and then treated with EEN, metronidazole, hydrocortisone, or EEN and metronidazole combination. Blood and tissue were collected at 2 and 4 weeks with histology, mucosal integrity, tight junction integrity, inflammation, and H. trogontum load evaluated. Results . H. trogontum induced colitis in IL-10 −/− mice with histological changes in the cecum and colon. Elevated mucosal IL-8 mRNA in infected mice was associated with intestinal barrier dysfunction indicated by decreased transepithelial electrical resistance and mRNA of tight junction proteins and increased short-circuit current, myosin light chain kinase mRNA, paracellular permeability, and tumor necrosis factor- α and myeloperoxidase plasma levels (<mml:math xmlns:mml=http://www.w3.org/1998/Math/MathML id=M1><mml:mi>P</mml:mi><mml:mo><</mml:mo><mml:mn>0.01</mml:mn></mml:math>for all comparisons). EEN and metronidazole, but not hydrocortisone, treatments restored barrier function, maintained gut barrier integrity, and reversed inflammatory changes along with reduction of H. trogontum load (versus infected controls<mml:math xmlns:mml=http://www.w3.org/1998/Math/MathML id=M2><mml:mi>P</mml:mi><mml:mo><</mml:mo><mml:mn>0.05</mml:mn></mml:math>). Conclusion . H. trogontum infection in IL-10 −/− mice induced typhlocolitis with intestinal barrier dysfunction. EEN and metronidazole, but not hydrocortisone, modulate barrier dysfunction and reversal of inflammatory changes." @default.
• W2163675591 created "2016-06-24" @default.
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• W2163675591 date "2013-01-01" @default.
• W2163675591 modified "2023-09-27" @default.
• W2163675591 title "Inflammatory Bowel Disease Therapies and Gut Function in a Colitis Mouse Model" @default.
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• W2163675591 doi "https://doi.org/10.1155/2013/909613" @default.
• W2163675591 hasPubMedCentralId "https://www.ncbi.nlm.nih.gov/pmc/articles/3763566" @default.
• W2163675591 hasPubMedId "https://pubmed.ncbi.nlm.nih.gov/24027765" @default.
• W2163675591 hasPublicationYear "2013" @default.
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